Human DNA (cytosine-5)-methyltransferases: a functional and structural perspective for epigenetic cancer therapy

Grégoire Rondelet; Johan Wouters

doi:10.1016/j.biochi.2017.06.003

Human DNA (cytosine-5)-methyltransferases: a functional and structural perspective for epigenetic cancer therapy

Grégoire Rondelet, Johan Wouters (Promoteur)

Résultats de recherche: Contribution à un journal/une revue › Article de revue

Résumé

Epigenetic modifications modulate chromatin states to regulate gene expression. Among them, DNA methylation and histone modifications play a crucial role in the establishment of the epigenome. In cancer, these epigenetic events may act in concert to repress tumor suppressor genes or promote oncogenic pathways. In the context of cancer initiation and progression, recruitment of DNA (cytosine-5)-methyltransferases to specific genomic regions is mainly mediated by histone epigenetic marks, transcription factors and co-regulators as part of a dynamic process. Herein, we will review these mechanisms and present state-of-the-art of DNA methylation, treatment and development of epigenetic cancer therapies targeting this epigenetic modification.

langue originale	Anglais
Numéro d'article	139
Pages (de - à)	137-147
Nombre de pages	11
journal	Biochimie
Volume	139
Les DOIs	https://doi.org/10.1016/j.biochi.2017.06.003
Etat de la publication	Publié - 1 août 2017

Accès au document

10.1016/j.biochi.2017.06.003

Link to publication in Scopus

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Contient cette citation

Rondelet, G., & Wouters, J. (2017). Human DNA (cytosine-5)-methyltransferases: a functional and structural perspective for epigenetic cancer therapy. Biochimie, 139, 137-147. [139]. https://doi.org/10.1016/j.biochi.2017.06.003

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abstract = "Epigenetic modifications modulate chromatin states to regulate gene expression. Among them, DNA methylation and histone modifications play a crucial role in the establishment of the epigenome. In cancer, these epigenetic events may act in concert to repress tumor suppressor genes or promote oncogenic pathways. In the context of cancer initiation and progression, recruitment of DNA (cytosine-5)-methyltransferases to specific genomic regions is mainly mediated by histone epigenetic marks, transcription factors and co-regulators as part of a dynamic process. Herein, we will review these mechanisms and present state-of-the-art of DNA methylation, treatment and development of epigenetic cancer therapies targeting this epigenetic modification.",

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N2 - Epigenetic modifications modulate chromatin states to regulate gene expression. Among them, DNA methylation and histone modifications play a crucial role in the establishment of the epigenome. In cancer, these epigenetic events may act in concert to repress tumor suppressor genes or promote oncogenic pathways. In the context of cancer initiation and progression, recruitment of DNA (cytosine-5)-methyltransferases to specific genomic regions is mainly mediated by histone epigenetic marks, transcription factors and co-regulators as part of a dynamic process. Herein, we will review these mechanisms and present state-of-the-art of DNA methylation, treatment and development of epigenetic cancer therapies targeting this epigenetic modification.

AB - Epigenetic modifications modulate chromatin states to regulate gene expression. Among them, DNA methylation and histone modifications play a crucial role in the establishment of the epigenome. In cancer, these epigenetic events may act in concert to repress tumor suppressor genes or promote oncogenic pathways. In the context of cancer initiation and progression, recruitment of DNA (cytosine-5)-methyltransferases to specific genomic regions is mainly mediated by histone epigenetic marks, transcription factors and co-regulators as part of a dynamic process. Herein, we will review these mechanisms and present state-of-the-art of DNA methylation, treatment and development of epigenetic cancer therapies targeting this epigenetic modification.

KW - DNA methylation

KW - Promoter methylation

KW - Gene body methylation

KW - protein-protein interaction

KW - DNMT inhibitors

KW - Epigenetic therapy

KW - Protein-protein interaction

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DO - 10.1016/j.biochi.2017.06.003

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